As a result of previous experimental studies we have proposed the concept that gastric ulcers are caused by a hypersecretion of gastric juice of hormonal origin brought about by stasis of food in the stomach as a result of pyloric stenosis or gastric atony. This view has been challenged by DuPlessis and Capper who suggest that gastric ulcers are not acid-peptic in origin but are caused by regurgitation of bile and pancreatic juice into the stomach. To test this theory we have diverted bile and pancreatic juice into the stomach and esophagus of dogs by a modified Mann-Williamson procedure. This diversion did not produce ulcers in the esophagus or stomach in seven months. However, the dog is quite resistant to peptic ulceration so we wish to repeat these studies in swine, an animal that occasionally has chronic gastric ulcers. We plan also to test the corrosive properties of bile by implanting various organs into the gallbladder and by testing the effect of the duodenal secretions on the legs of living frogs. Present work on the mechanism of gastrin release will be continued as well as studies on afferent fibers in the vagus nerves.